Biomedical Engineering Reference
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surgical patients (Fig. 1) . Inactivation of NO by L-NMMA results in high CAM
expression, indicating that NO is an important inhibitor of CAM expression and
EC-PMN interactions (Yeh et al. 2007). In an established septic animal study also
performed by our laboratory, mice were assigned to a control group or an Arg
group. h e control group was fed a common semipurii ed diet, whereas 2% of total
calories in the diet was provided by Arg in the Arg group. At er 3 wk, sepsis was
induced in both groups of mice by cecal ligation and puncture. h e results showed
that compared to the control group, pretreatment with an Arg-supplemented
diet resulted in higher plasma ICAM-1 levels and leukocyte CD11a/CD18 and
CD11b/CD18 expression during sepsis (Table 1) . h e Arg group had higher
myeloperoxidase activities in various organs at 24 hr at er sepsis. Myeloperoxidase
is a neutrophil-specii c enzyme and is considered to be an index of neutrophil
ini ltration. h ese results indicated that Arg administration may aggravate the
inl ammatory reaction and increase neutrophil ini ltration into tissues (Yeh et al.
2006). h e adverse ef ects of Arg on the inl ammatory reaction observed in that
study were distinct from previous Arg supplementation studies with benei cial
results. Many factors may contribute to the inconsistent ef ects of enteral Arg
supplementation. Previous reports suggested that NO can have dif erential ef ects
on dif erent stages of leukocyte recruitment and CAM expression, depending
on the levels produced. h e amount and timing of Arg supplementation and the
characteristics and the severity of various diseases may result in dif erent levels of
NO and NO-related cytotoxic substances. h is may partly explain the discrepancies
between experiments.
Table 1
Effects of Arg on leukocyte CD11a/CD18 and CD11b/CD18 expression during
sepsis
CD 11a/CD 18%
CD 11b/CD 18(%)
NC
5.23 ± 1.65
9.56 ± 1.98
0 h
Control
4.87 ± 1.61
10.78 ± 0.26
Arg
4.08 ± 0.24
11.38 ± 1.74
6 h
Control
19.58 ± 1.25 †.‡
3.6 ± 1.51
14.65 ± 1.96*.
17.2 ± 1.94
Arg
12 h
Control 3.06 ± 1.79 13.68 ± 0.54 †.‡
Arg 25.38 ± 4.5*. 25.22 ± 2.16*. †.‡
Control 6.13 ± 2.45 9.83 ± 0.59
Arg 43.03 ± 3.28*. †.‡ 26.2 ± 1.39*. †.‡
Leukocyte integrins CD11a/CD18 and CD11b/CD18 expressions were signii cantly higher in the Arg group 12, and
24 hr at er sepsis than those of the corresponding control and the normal control (NC) group. Results are presented
as mean ± SD. *Dif erent from the control group at the same time point. Reprinted from Yeh et al. (2006), with
permission.
 
 
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